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环孢素诱导Wistar大鼠出现类糖尿病综合征及其停药后的可逆性。

Induction of a diabetes-like syndrome by cyclosporine in Wistar rats and its reversibility after drug withdrawal.

作者信息

Hahn H J, Kauert C, Kotzke G

机构信息

Central Institute of Diabetes, Research and Treatment, Karlsburg, GDR.

出版信息

Exp Clin Endocrinol. 1987 Aug;90(1):46-50. doi: 10.1055/s-0029-1210671.

DOI:10.1055/s-0029-1210671
PMID:3311780
Abstract

Cyclosporin A exerts dose- and time-related toxic effects on pancreatic B-cells. We investigated the reversibility of Cyclosporin A-induced alterations on glucose tolerance and pancreatic insulin content in Wistar rats either still normoglycaemic or animals being hyperglycaemic after different treatment periods. Both groups of animals either formerly normoglycaemic but glucose intolerant or hyperglycaemic normalized glucose intolerance, glycaemia and reenhanced pancreatic insulin content. This demonstrates that also hyperglycaemic animals are able to recover spontaneously from a diabetes-like state.

摘要

环孢素A对胰腺β细胞产生剂量和时间相关的毒性作用。我们研究了在不同治疗期后仍血糖正常或已出现高血糖的Wistar大鼠中,环孢素A诱导的葡萄糖耐量和胰腺胰岛素含量改变的可逆性。两组动物,无论是先前血糖正常但葡萄糖不耐受的,还是高血糖的,均使葡萄糖不耐受、血糖水平正常化,并提高了胰腺胰岛素含量。这表明高血糖动物也能够从类似糖尿病的状态中自发恢复。

相似文献

1
Induction of a diabetes-like syndrome by cyclosporine in Wistar rats and its reversibility after drug withdrawal.环孢素诱导Wistar大鼠出现类糖尿病综合征及其停药后的可逆性。
Exp Clin Endocrinol. 1987 Aug;90(1):46-50. doi: 10.1055/s-0029-1210671.
2
Subcutaneous cyclosporin prevents the development of complete Freund's adjuvant-streptozotocin-induced diabetes in the rat.皮下注射环孢素可预防大鼠因完全弗氏佐剂-链脲佐菌素诱导的糖尿病的发生。
Diabete Metab. 1991 Mar-Apr;17(2):281-5.
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Morphology of the endocrine pancreas in cyclosporine-treated glucose-intolerant Wistar rats.环孢素处理的糖耐量异常Wistar大鼠内分泌胰腺的形态学
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Is the cyclosporin A toxicity on rat pancreatic B-cells modulated by the MHC?环孢素A对大鼠胰腺β细胞的毒性是否受主要组织相容性复合体(MHC)的调节?
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Diabetes Res. 1986 Mar;3(3):161-7.

引用本文的文献

1
Cyclosporine pharmacokinetics and effect in the type I diabetic rat model.环孢素在I型糖尿病大鼠模型中的药代动力学及效应
Eur J Drug Metab Pharmacokinet. 1989 Oct-Dec;14(4):287-92. doi: 10.1007/BF03190113.